Nutrition research and practice · 2026
Chrysanthemum morifolium extract prevents oxidative stress and ferroptosis in cerebral ischemia-reperfusion injury by modulating the miR-144/Nrf2 pathway.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Jiang Yin, Li Bo, Zhang Zheng, Yang Jie, Chen JianE, Li Yan
Аннотация
BACKGROUND/OBJECTIVES: Cerebral ischemia-reperfusion injury (CIRI) is characterized by oxidative stress (OS) and ferroptosis. Chrysanthemum morifolium extract (CME) has been reported to have antioxidant activity. This study evaluated its protective effects and underlying mechanisms against CIRI.
MATERIALS/METHODS: In vitro, H19-7 cells were pretreated with CME before oxygen-glucose deprivation/reoxygenation (OGD/R). Cell viability, apoptosis, OS markers (reactive oxygen species [ROS], malondialdehyde [MDA], glutathione [GSH], and superoxide dismutase [SOD]), ferroptosis markers, and the related proteins of the miR-144/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway were assessed. The targeting relationship between miR-144 and Nrf2 was confirmed by dual-luciferase reporter assay. Rescue experiments were performed using Nrf2 overexpression. An in vivo rat middle cerebral artery occlusion (MCAO) model was established, and the effects of CME, agomir-144 (miR-144 agonist), and bardoxolone (BARD; Nrf2 agonist) on the cerebral infarct volume, histopathology, apoptosis, and the aforementioned molecular pathways were evaluated.
RESULTS: A CME pretreatment significantly restored the cell viability, reduced apoptosis, and suppressed OS and ferroptosis in OGD/R-induced H19-7 cells, as evidenced by decreased ROS, MDA, apoptosis, lipid peroxidation, and Fe2+ levels, and increased GSH, SOD, and the expression of nuclear Nrf2 and its downstream proteins (heme oxygenase-1, glutamate-cysteine ligase modifier subunit, solute carrier family 7 member 11, and glutathione peroxidase 4). These protective effects were reversed by miR-144 mimic but rescued by Nrf2 overexpression. Consistently, the in vivo results showed that CME reduced cerebral infarction, ameliorated neuronal damage and apoptosis in MCAO rats, and modulated the miR-144/Nrf2 pathway and related OS/ferroptosis markers. Agomir-144 attenuated these benefits, while a BARD co-treatment restored them.
CONCLUSION: CME alleviates CIRI by inhibiting OS and ferroptosis via the miR-144/Nrf2 pathway, providing novel insights into CIRI treatment strategies.
MATERIALS/METHODS: In vitro, H19-7 cells were pretreated with CME before oxygen-glucose deprivation/reoxygenation (OGD/R). Cell viability, apoptosis, OS markers (reactive oxygen species [ROS], malondialdehyde [MDA], glutathione [GSH], and superoxide dismutase [SOD]), ferroptosis markers, and the related proteins of the miR-144/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway were assessed. The targeting relationship between miR-144 and Nrf2 was confirmed by dual-luciferase reporter assay. Rescue experiments were performed using Nrf2 overexpression. An in vivo rat middle cerebral artery occlusion (MCAO) model was established, and the effects of CME, agomir-144 (miR-144 agonist), and bardoxolone (BARD; Nrf2 agonist) on the cerebral infarct volume, histopathology, apoptosis, and the aforementioned molecular pathways were evaluated.
RESULTS: A CME pretreatment significantly restored the cell viability, reduced apoptosis, and suppressed OS and ferroptosis in OGD/R-induced H19-7 cells, as evidenced by decreased ROS, MDA, apoptosis, lipid peroxidation, and Fe2+ levels, and increased GSH, SOD, and the expression of nuclear Nrf2 and its downstream proteins (heme oxygenase-1, glutamate-cysteine ligase modifier subunit, solute carrier family 7 member 11, and glutathione peroxidase 4). These protective effects were reversed by miR-144 mimic but rescued by Nrf2 overexpression. Consistently, the in vivo results showed that CME reduced cerebral infarction, ameliorated neuronal damage and apoptosis in MCAO rats, and modulated the miR-144/Nrf2 pathway and related OS/ferroptosis markers. Agomir-144 attenuated these benefits, while a BARD co-treatment restored them.
CONCLUSION: CME alleviates CIRI by inhibiting OS and ferroptosis via the miR-144/Nrf2 pathway, providing novel insights into CIRI treatment strategies.